Binge eating is a prominent characteristic of most eating disorders. A history of caloric restriction and the over-consumption of highly palatable foods are two main variables that participate in the state-dependent perpetuation of bingeing behavior. The objective of the current project is to investigate alterations that occur in the mu-opioid control of the caudal brainstem function in female rats exposed to a repeated cycle of calorie restriction and access to palatable foods. The proposed hypothesis is that a history of binge-like eating results in alterations in gastrointestinal sensory feedback, which are mediated, in part, through central opioid mechanisms. The hypothesis will be tested by using in situ hybridization labeling of the mu-opioid receptor mRNA, immunohistochemical staining of the protein product of the early immediate gene, c-Fos, and neuro-electrophysiological techniques. These approaches will allow us to determine how binge-like eating alters caudal brai nstem mu-opioid receptors (Specific Aim 1). In addition, we will determine how central mu-opioid activity alters feeding, neuronal activation (Specific Aim 2), and single unit activity of GI responsive neurons in the nucleus of the solitary tract to gastric loads (Specific Aim 3). The long-term objective of this line of research is to understand how repeated cycles of calorie restriction and access to palatable foods leads to alterations in the neural mechanisms involved in the homeostatic processes of food intake. This project is unique in that it will assess the caudal brainstem sensory adaptations to the maintenance of binge-like eating. The findings from this project, therefore, will be especially relevant for the identification of sustaining factors and potential treatments for binge-related eating disorders, bulimia nervosa (BN) and binge eating disorder (BED).